Ebola Hemorrhagic Fever (EHF)
Introduction Ebola, previously known as Ebola hemorrhagic fever, was first discovered in 1976 after Epidemic of Ebola hemorrhagic fever (rare and deadly disease) occurred near the Ebola River in Zaire (what is now the Democratic Republic of the Congo) and Sudan. More than 500 cases were reported in the outbreaks and approximately 400 deaths due to clinical hemorrhagic fever. Hospital staffs are more susceptible to infection in any outbreak, due to close proximity and contact with patients’ blood and excreta. Other reported cases of outbreaks of Ebola occurred in Uganda (2000), the Republic of the Congo (1995,2001,2002,2003), Sudan (2004), Gabon (1994,1996,1997, 2002), South Africa (1996) and Angola (2005). The 2003 outbreak was first recognized by death of gorillas and chimpanzees in large numbers. The current and most severe outbreak of Ebola in West Africa (Guinea, Sierra Leone, and Liberia) was first reported in March 2014 and reportedly spreading across Africa to other part of the world. On August 8, 2014 the World Health Organization Director-General declared the outbreak a Public Health Emergency of International Concern. Ebola is caused by infection with Filoviruses that belong to a virus family called Filoviridae, genus Ebola virus a highly virulent in humans and nonhuman primates and can cause severe hemorrhagic fever, with infection ending in death. Only two highly virulent members of this virus family have been identified: Marburg (Marburg disease was recognized in 1967 in laboratory workers in Germany and Yugoslavia were exposed to tissues of African green Monkeys) and Ebola viruses. In Marburg disease the incubation period is 3-9 days and incubation period of 2-21days for Ebola. There five identifiable subtypes of Ebola virus species, four of which causes disease in humans: Taï Forest virus (formerly Ivory Coast), Sudan, Zaire, Bundibugyo viruses (CDC, 2014). The fifth, Ebola Reston virus is the only known Filovirus to have cause severe disease in primates (e.g. monkeys), but not in humans. Reston virus was first detected in 1989, in cynomolgus monkeys (Macaca fascicularis) ''that was imported and held in quarantine facility in Virginia United States from the Philippines. Infection spread to proximately 149 persons in contact with the infected monkeys or their tissues, but none of the works became sick, indicating that Reston virus possesses low pathogenicity in humans. Humans exposure to Ebola is as a result of close contact with the blood, secretions, organs and other bodily fluids of infected animals such as chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines found ill or dead or in the rainforest. Ebola infection appears to be immunosuppressive, fatal and highest mortality rates of 25-90%. Structure/Genome * The Ebola genome is single-stranded, non-segmented, negative sense RNA (encased in the nucleocapside and enveloped in a lipid bilayer membrane), about 18-19kb in size and contain seven genes. * Ebola structure consists of cell membrane, outer glycoproteins, and nuclear proteins inside. * The genetic material, which is RNA, is within the nuclear protein. Ebola also has an enzyme called polymerase, which helps in its replication. * Some of the structural proteins associated with the nucleocapside are the nucleoprotein (NP), VP30, VP35, and the polymerase (L) protein. * Membrane associated proteins are VP40 (matrix protein), VP24, and the GP (peplomer glycoprotein). Glycoprotein makes up the viral surface spikes in the form of trimmers 10 nm in length. Virons are released via budding from the plasma membrane. The viral RNA dependent RNA polymerase binds the encapsulated genome at the 3’ OH of the leader region, and sequentially transcribe each genes starting from the start site and end with capped mRNAs and transcriptional stop (Polyadenylation site) at the 5’ trailer sequence. The envelope glycoprotein (GP) is encoded in two reading frames and requires transcriptional editing or translational frame shifting to be expressed. The primary gene product of the unedited transcript of GP gene yields sGP, a nonstructural secreted glycoprotein from infected cells. Replication * Ebola virus attaches to host receptors cell using a glycoprotein called a peplomer. * A peplomer is a glycoprotein spike on a viral envelope that binds to specific receptors on host cell (essential for specificity and viral infectivity). * The virus is internalized via macropinocytosis (type of endocytic vesicles) is then engulfed by endocytosis. * Ebola virion envelope and cellular membrane of host fuses together and the virus nucleocapside is released. * Virus uncoats and the nucleocapside is transcribed onto positive stranded mRNA, which is translated into viral proteins. * Glycosylation occurs in which viral proteins attach to glycan and the glycoprotein precursors are cleaved into glycoprotein 1 and 2. Glycoproteins 1 and 2 assemble to form heterodimers. * A negative stranded RNA strand is synthesized and used as a template to create positive single stranded RNA. * Heterodimers multiply to form trimmers that will form the surface peplomers of the emerging Ebola cells. New viral RNA copies are made or replicated (using RNA polymerase) from the negative stranded RNA strand and the trimmers make their way to the cell membrane. * Formation of nucleocapsids and viral envelope occur when the trimmers (viral proteins) and new genome gather around the edges of the host cell in preparation for budding. * Newly formed Ebola viruses bud from the host cell, gaining the cell’s membrane and the mature progeny are free and ready to infect other cells. Transmission/Risk of exposure Ebola transmission into human population is through direct contact with infected animal, such fruit bats, monkeys, chimpanzees, gorillas and other infected primates. The virus then spillover through person-to-person transmission via direct contact, secretion, blood and other bodily fluids (urine, saliva, sweat, feces, vomit, breast milk, and semen) of an infected person, objects and materials. According to CDC, “Ebola is not spread through the air, by water, or in general, by food.” Symptoms Symptoms develop from 2 -21days (average 8-10days) after exposure to Ebola. Early symptoms of Ebola include: * Fever greater than 101.5°F (38.6°C) * Chills * Severe headache * Sore throat * Rash * Red eyes * Muscle pain * Weakness * Abdominal (stomach) pain * Diarrhea * Vomiting Late symptoms include: * Unexplained hemorrhage (bleeding or bruising) * Bleeding from the mouth and rectum * Bleeding from eyes, ears, and nose * Organ failure Diagnosis * Signs and symptoms of Ebola are suspected * investigation methods: * antibody-capture enzyme-linked immunosorbent assay (ELISA) * antigen-capture detection tests * serum neutralization test * reverse transcriptase polymerase chain reaction (RT-PCR) assay * electron microscopy * virus isolation by cell culture. Prevention and Treatments No known cure for Ebola, but experimental treatments has been used, however none have been fully tested or understood. '''Prevention:' * Infected person(s) must be isolated to avoid spreading the disease. * Health care profession should be contacted. * Survival depends person (s) immune system responds to the virus * Survival(s) of Ebola are immune from the virus for Ten years or more, and can no longer spread the virus * Men who survived the infection can carry the Ebola virus in their sperm approximately three months or longer. The use of condom or abstain from sex within this period is recommended. * Some of the long-term complications include joint and vision problems Treatment for Ebola includes: * Fluids given through a vein (IV) * Oxygen * Blood pressure management * Treatment for other infections * Blood transfusions References Ebola (Ebola Virus Disease). (2014, November 26). Retrieved November 28, 2014, from Centers for Disease Control and Prevention Ebola virus disease: MedlinePlus Medical Encyclopedia. (2014, January 1). Retrieved November 29, 2014 Filoviridae. (2014, April 7). Retrieved November 28, 2014. MEDICAL: Steps towards fighting Ebola virus. (n.d.). Retrieved November 29, 2014 Mühlberger, E. (2007). Filovirus replication and transcription. Future Virology, 2(2), 205–215. doi:10.2217/17460794.2.2.205 Peters, C., & Peters, J. (n.d.). An Introduction to Ebola: The Virus and the Disease. National Center for Infectious Diseases, Centers for Disease Control and Prevention. Retrieved November 24, 2014. Review of Human-to-Human Transmission of Ebola Virus. (2014, October 29). Retrieved November 29, 2014. ViralZone: Ebolavirus replication cycle. (2014, January 1). Retrieved November 29, 2014.